Fig 2: Proportion of fibroblasts expressing HtrA1 protein in keloid lesions and normal skin. The number of fibroblasts with positive signals was counted after immunohistochemical staining of HtrA1 using samples from 17 keloidand 4 unrelated patients. Ten high-power (×400) fields were selected at random from a section and numbers of total and stained fibroblasts were counted. Patient information is described with proportion of HtrA1-positive cells in Table 1.

Fig 3: Effects of DNA methyltransferase and histone deacetylase inhibitors on HtrA1 transcript levels in human breast cancer cell lines.The indicated cell lines were treated with the DNA methyltransferase inhibitor decitabine (DEC) and/or with the histone deacetylase inhibitor TSA, as described, and resultant effects on HtrA1 transcript levels were determined using QPCR. Values ± SEs are shown from a representative experiment, which was repeated 2 times. Values for Dec and TSA were significant at p<0.01 for the MDA-MB-231 and -468 cell lines. Inset shows an expanded view of the MCF7 and M4A4 results.

Fig 4: An abdominal keloid after laparoscopic surgery. The activity of keloid was in order a, b and c. Higher activity in regions of the lesion were associated with increased cell proliferation and greater up-regulation of HtrA1. Scale bar = 500 µm.

Fig 5: Western blot analysis of HtrA1 in keloid lesions and normal skin tissues. Soluble protein extract (8 µg/lane) was analysed using specific antibodies against HtrA1 or glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Keloid and normal skin samples from four different patients were analysed.